The torso response element binds GAGA and NTF-1/Elf-1, and regulates tailless by relief of repression
The torso response element binds GAGA and NTF-1/Elf-1, and regulates tailless by relief of repression
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DOI：
10.1101/gad.9.24.3163
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发表时间：
1995-12-15
影响因子：
10.5
通讯作者：
Lengyel, JA
中科院分区：
文献类型：
--
作者：
Liaw, GJ;Rudolph, KM;Lengyel, JA
转录因子活性的调节导致细胞行为的改变（例如，分化与增殖）是受体酪氨酸激酶（RTK）刺激的关键结果之一。在果蝇早期胚胎中，胚胎两极的 torso（tor）RTK的激活引发一个磷酸化级联反应，导致无尾（tll）基因的空间特异性转录。我们对tll启动子中tor反应元件（tor - RE）的分析表明，由tor RTK途径调节的关键活性是一种存在于整个胚胎中的阻遏物。我们已将tor - RE定位到一个11bp的序列；以该序列为基础进行蛋白质纯化，我们确定GAGA和NTF - 1（也称为Elf - 1，是grainyhead基因的产物）这两种蛋白质与tor - RE结合。我们证明NTF - 1可被MAPK（丝裂原活化蛋白激酶）磷酸化，并且在缺乏母源NTF - 1活性的胚胎中tll表达扩大；这些结果使NTF - 1成为体内tor RTK途径调节的一个可能靶点。这里呈现的数据支持一种模型，即胚胎两极的tor RTK激活导致阻遏物失活，从而使胚胎两极的tll基因（通过存在于整个胚胎中的激活因子）转录激活。
Modulation of transcription factor activity leading to changes in cell behavior (e.g., differentiation versus proliferation) is one of the critical outcomes of receptor tyrosine kinase (RTK) stimulation. In the early Drosophila embryo, activation of the torso (tor) RTK at the poles of the embryo activates a phosphorylation cascade that leads to the spatially specific transcription of the tailless (tll) gene. Our analysis of the tor response element (tor-RE) in the tll promoter indicates that the key activity modulated by the tor RTK pathway is a repressor present throughout the embryo. We have mapped the tor-RE to an 11-bp sequence; using this sequence as the basis for protein purification, we have determined that the proteins GAGA and NTF-1 (also known as Elf-1, product of the grainyhead gene) bind to the tor-RE. We demonstrate that NTF-1 can be phosphorylated by MAPK (mitogen-activated protein kinase), and that tll expression is expanded in embryos lacking maternal NTE-1 activity; these results make NTF-1 a likely target for modulation by the tor RTK pathway in vivo. The data presented here support a model in which activation of the tor RTK at the poles of the embryos leads to inactivation of the repressor and therefore, to transcriptional activation (by activators present throughout the embryo) of the tll gene at the poles of the embryo.